This article applies Bradford Hill’s criteria to assess whether raised visceral adipose tissue (VAT) is a causal driver of coronary heart disease rather than a passive marker of obesity. Drawing on imaging cohorts, prospective studies, Mendelian randomisation, mechanistic biology, and interventional evidence, it shows that VAT meets key aspects of causality, including strength, consistency, temporality, dose–response, plausibility, and coherence. Visceral and epicardial fat exert pro-inflammatory, metabolic, and paracrine effects that promote atherogenesis independently of BMI. Although measurement variability and residual confounding remain, the totality of evidence supports VAT as a direct contributor to coronary risk, justifying VAT-targeted assessment and prevention strategies.

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